BACTERIAL EVASION OF IMMUNE DEFENSE
There are several ways in which bacteria can survive in the host by evasion of the immune defenses. These mechanisms will be briefly summarized here, but the list of evasive mechanisms used by each bacterial species may be much longer in nature.
Capsules play an important role for long-term survival of pathogens. For example, group A streptococci have a hyaluronic acid capsule that is identical to hyaluronic acid in humans. While antibod-ies can be obtained following immuniza-tion with the streptococcal hyaluronic acid, they are nonprecipitating antibodies and are not effective in eliminating the organ-ism. Polysaccharide antigens of both the pneumococcus and the meningococcus capsules can inhibit phagocytosis of the organism and mucoid secretions of these polysaccharides can block the activation of the alternate pathway of complement.
Antigenic variation or drift is another mechanism whereby bacteria evade the immune system. The M protein (the most important virulence factor of the group A streptococcus) has been shown to exhibit antigen variation in the environment, and new M protein molecules appear regularly in human isolates of group A streptococci.
Another example is the relapsing fever by Borrelia. During the first episode, anti-bodies kill the bacteria and the fever sub-sides. However, some antigenic variants of the bacteria persist, and after five to seven days these new variants can cause a relapse in the patient with fever reap-pearing. Other examples of evasion of the immune response are bacteria such as N. gonorrhea, N. meningitidis, Haemophilus influenza, and others that secrete proteases that hydrolyze IgA antibody. Some strains of staphylococci secrete catalase, which prevents them from being killed inside phagocytic cells.
Table 4.2 List of All the Known Superantigens and Their Vβ Specificities
One must also consider that some bac-teria
sequester themselves in nonphago-cytic cells where they are not exposed to the
immune system. An excellent example is M.
tuberculosis, which can lie dormant for years inside a granulomatous, case-ous lesion
called the Ghon complex. Once ground up, live M. tuberculosis organism can be extracted from this complex.
Finally, a number of organisms display antigens on their surface that are cross-reactive with human antigens. This could result in an enhanced immune response to host tissue antigens or a diminished response secondary to similarities between bacterial and self-antigens.